Nephrology — MCQs

A 31-year-old woman experiences abdominal pain 1 week after noticing blood in her urine. She has had three episodes of urinary tract infection during the past year. Urinalysis shows 2+ hematuria, 1+ proteinuria, hypercalciuria, and no glucose or ketones. Microscopic examination of the urine shows numerous RBCs and oxalate crystals. An abdominal CT scan with contrast shows linear striations radiating into the renal papillae, along with small cystic collections of contrast material in dilated collecting ducts. She is advised to increase her daily intake of fluids, and her condition improves. Which of the following renal cystic diseases is most likely to be associated with these findings?

Q427Easy

Central nervous system manifestations in chronic renal failure are a result of all of the following except:

Q428Medium

In uremia, all of the following are reversed by dialysis except:

Q429Easy

What is the most common metabolic abnormality predisposing patients to renal stone formation?

Q430Easy

Rhabdomyolysis is seen in all of the following conditions except?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 421: What is the most common cause of chronic renal failure in adults?

A. Tuberculosis
B. Hypertension
C. Diabetes Mellitus (Correct Answer)
D. Glomerulonephritis

Explanation: **Explanation:** **1. Why Diabetes Mellitus is Correct:** Diabetes Mellitus (DM) is the leading cause of Chronic Kidney Disease (CKD) and End-Stage Renal Disease (ESRD) worldwide, accounting for approximately 40-50% of all cases [1]. The underlying pathophysiology involves chronic hyperglycemia leading to non-enzymatic glycosylation of the glomerular basement membrane, hyperfiltration injury, and the activation of the Renin-Angiotensin-Aldosterone System (RAAS) [2]. This results in characteristic Kimmelstiel-Wilson nodules (nodular glomerulosclerosis), eventually leading to progressive renal fibrosis and failure [2]. **2. Analysis of Incorrect Options:** * **Hypertension (Option B):** This is the **second** most common cause of chronic renal failure [1]. While hypertensive nephrosclerosis is a major contributor to renal decline, it statistically trails behind Diabetes. * **Glomerulonephritis (Option D):** This was historically a leading cause, but with better management and the global rise in metabolic syndrome, it now ranks third in most developed and developing nations. * **Tuberculosis (Option A):** While Genitourinary TB is a significant cause of chronic kidney injury in specific endemic regions (like parts of India) due to obstructive uropathy or parenchymal destruction, it is not the most common cause on a population-wide scale. **3. NEET-PG High-Yield Pearls:** * **Earliest Clinical Sign:** Microalbuminuria (30–300 mg/day) is the first sign of diabetic nephropathy [2]. * **Earliest Pathological Change:** Thickening of the Glomerular Basement Membrane (GBM) [2]. * **Pathognomonic Feature:** Kimmelstiel-Wilson (KW) nodules [2]. * **Management Tip:** ACE inhibitors or ARBs are the drugs of choice as they reduce intraglomerular pressure and provide renoprotection. * **Size Fact:** In diabetic nephropathy, kidneys are typically **enlarged** or normal-sized initially, unlike most other causes of CKD where kidneys are shrunken.

Question 422: All of the following are used for the treatment of hyperkalemia except?

A. Calcium gluconate
B. Sodium bicarbonate
C. Intravenous infusion of glucose with insulin
D. Beta blockers (Correct Answer)

Explanation: **Explanation:** The management of hyperkalemia focuses on three goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing potassium from the body [1]. **Why Beta-blockers are the correct answer:** Beta-blockers (specifically non-selective ones) **worsen** hyperkalemia. Under normal physiological conditions, $\beta_2$-adrenergic receptors stimulate the Na+/K+-ATPase pump, which drives potassium into the intracellular compartment. Beta-blockers inhibit this process, leading to an increase in serum potassium levels. In contrast, **$\beta_2$-agonists** (like nebulized Salbutamol) are used as a treatment to shift potassium into cells. **Analysis of other options:** * **Calcium gluconate:** This is the first-line treatment for hyperkalemia with ECG changes [1]. It does not lower potassium levels but **stabilizes the myocardial membrane** by antagonizing the effects of potassium on the cardiac conduction system [1]. * **Sodium bicarbonate:** It promotes the movement of potassium into cells by increasing the blood pH (alkalosis). As hydrogen ions ($H^+$) move out of cells to buffer the alkalosis, potassium ($K^+$) moves into the cells to maintain electroneutrality. * **IV Glucose with Insulin:** Insulin is a potent stimulator of the Na+/K+-ATPase pump. Glucose is co-administered to prevent hypoglycemia. This is one of the fastest ways to shift potassium intracellularly. **NEET-PG Clinical Pearls:** 1. **"C Big K" Mnemonic** for treatment: **C**alcium gluconate, **B**icarbonate, **I**nsulin/Glucose, **G**-agonists (Salbutamol), **K**ayexalate (Resins), and **K**idney dialysis. 2. **Calcium gluconate vs. Calcium chloride:** Calcium gluconate is preferred via peripheral lines as it is less caustic to veins. 3. **Definitive removal:** While insulin and bicarbonate shift potassium, **Loop diuretics** and **Hemodialysis** are required for actual elimination from the body.

Question 423: Hypertension with hypokalemia is typically seen in which of the following conditions?

A. Bartter Syndrome
B. Liddle's Syndrome (Correct Answer)
C. Gitelman's Syndrome
D. All of the above

Explanation: ### Explanation The combination of **hypertension and hypokalemia** is a classic presentation of mineralocorticoid excess (either real or apparent). [2] **1. Why Liddle’s Syndrome is Correct:** Liddle’s Syndrome is an autosomal dominant disorder caused by a "gain-of-function" mutation in the **ENaC (Epithelial Sodium Channels)** in the collecting tubules. This leads to constitutive sodium reabsorption and potassium excretion. * **Mechanism:** Increased sodium reabsorption leads to volume expansion and **hypertension**. * **Biochemical Profile:** The volume expansion suppresses the Renin-Angiotensin-Aldosterone System (RAAS), resulting in **low renin and low aldosterone** (Pseudo-hyperaldosteronism). [3] The increased distal delivery of sodium drives potassium secretion, causing **hypokalemia**. [1] **2. Why Other Options are Incorrect:** * **Bartter Syndrome:** This is a "salt-wasting" tubulopathy affecting the thick ascending limb (NKCC2 transporter). It presents with hypokalemia and metabolic alkalosis, but patients are **normotensive or hypotensive** due to salt loss and have high renin/aldosterone levels. * **Gitelman’s Syndrome:** Similar to Bartter, this is a salt-wasting disorder affecting the distal convoluted tubule (NCCT transporter). It presents with hypokalemia, hypomagnesemia, and hypocalciuria, but patients are **normotensive**. **3. High-Yield Clinical Pearls for NEET-PG:** * **Liddle’s Treatment:** Does not respond to Spironolactone (since aldosterone is already low). It is treated with ENaC blockers like **Amiloride or Triamterene**. * **Differential for HTN + Hypokalemia:** * *High Aldosterone, Low Renin:* Primary Hyperaldosteronism (Conn’s Syndrome). [2] * *Low Aldosterone, Low Renin:* Liddle’s Syndrome, Cushing’s Syndrome, or Licorice ingestion (AME). [3] * **Mnemonic:** Bartter’s is like a "Loop diuretic" (Loop of Henle), Gitelman’s is like a "Thiazide diuretic" (Distal tubule). Both cause low BP; Liddle’s is the opposite.

Question 424: A patient presents with hematuria for many days. Investigations reveal renal calculi, calcifications in the wall of the urinary bladder, and a small contracted bladder. What is the most probable cause?

A. Schistosomiasis (Correct Answer)
B. Amyloidosis
C. Tuberculosis
D. Carcinoma of the urinary bladder

Explanation: ### Explanation The clinical triad of **hematuria**, **bladder wall calcification**, and a **small contracted bladder** in the presence of renal calculi is a classic presentation of **Schistosomiasis** (specifically *Schistosoma haematobium*) [1]. #### Why Schistosomiasis is Correct? * **Pathogenesis:** The adult flukes reside in the perivesical venous plexus [1]. Eggs are deposited in the bladder wall, inducing a granulomatous reaction and chronic inflammation. * **Calcification:** As the eggs die, they undergo calcification. On imaging, this appears as a characteristic "fetal head" or linear calcification of the bladder wall. * **Contracted Bladder:** Chronic inflammation leads to extensive fibrosis, reducing bladder capacity and compliance (thimble bladder). * **Calculi:** Urinary stasis and the presence of calcified eggs acting as a nidus frequently lead to secondary stone formation [3]. #### Why Other Options are Incorrect? * **Tuberculosis (TB):** While TB causes a "thimble bladder" and hematuria, the calcification in TB typically involves the **renal parenchyma** (putty kidney) or ureters rather than the bladder wall itself [3]. * **Amyloidosis:** Can cause bladder thickening and hematuria [2], but diffuse bladder wall calcification is not a characteristic feature. * **Carcinoma of the Bladder:** While *S. haematobium* is a risk factor for **Squamous Cell Carcinoma**, the primary presentation of a tumor is a filling defect or mass rather than diffuse wall calcification and contraction. #### High-Yield Clinical Pearls for NEET-PG * **Vector:** *Bulinus* snail. * **Infective stage:** Cercaria (penetrates skin during swimming) [1]. * **Diagnostic feature:** Terminal spined eggs in urine. * **Malignancy Risk:** Strongly associated with **Squamous Cell Carcinoma** of the bladder (unlike the more common Transitional Cell Carcinoma). * **Drug of Choice:** Praziquantel.

Question 425: Nephrocalcinosis is a feature of which of the following conditions?

A. Primary hyperparathyroidism
B. Medullary sponge kidney
C. Vitamin D intoxication
D. Pseudohypoparathyroidism (Correct Answer)

Explanation: Explanation: **Nephrocalcinosis** refers to the generalized deposition of calcium salts within the renal parenchyma (medulla or cortex). **Why Pseudohypoparathyroidism (PHP) is the correct answer:** In PHP, there is end-organ resistance to Parathyroid Hormone (PTH). This leads to **hypocalcemia** and **hyperphosphatemia**. To manage this, patients are treated with high doses of Vitamin D and calcium [1]. However, because these patients lack the phosphaturic effect of PTH and often have a high calcium-phosphate product, they are highly prone to developing **hypercalciuria** and subsequent nephrocalcinosis during treatment [1]. It is a classic, high-yield association in renal and endocrine pathology. **Analysis of Incorrect Options:** * **A. Primary Hyperparathyroidism:** While this causes hypercalcemia and hypercalciuria, it is more commonly associated with **nephrolithiasis** (kidney stones) rather than diffuse nephrocalcinosis, though the latter can occur in severe, chronic cases [2]. * **B. Medullary Sponge Kidney (MSK):** MSK is characterized by cystic dilatation of the collecting ducts. While it predisposes to stones and localized calcifications, it is fundamentally a structural malformation. * **C. Vitamin D Intoxication:** This leads to hypercalcemia and hypercalciuria [2]. While it *can* cause nephrocalcinosis, in the context of standard NEET-PG questions, PHP is the more specific "textbook" association often tested regarding its paradoxical relationship with calcium deposition despite low serum calcium. **High-Yield Clinical Pearls for NEET-PG:** * **Distinction:** Nephrocalcinosis (diffuse parenchymal) vs. Nephrolithiasis (stones in the pelvicalyceal system). * **Most common cause of Medullary Nephrocalcinosis:** Distal Renal Tubular Acidosis (Type 1 RTA). * **Albright’s Hereditary Osteodystrophy:** The phenotypic presentation of PHP Type 1a (short stature, round face, short 4th/5th metacarpals). * **Radiology:** The "eggshell" calcification or "stippled" appearance in the renal pyramids is characteristic of medullary nephrocalcinosis.

Question 426: A 31-year-old woman experiences abdominal pain 1 week after noticing blood in her urine. She has had three episodes of urinary tract infection during the past year. Urinalysis shows 2+ hematuria, 1+ proteinuria, hypercalciuria, and no glucose or ketones. Microscopic examination of the urine shows numerous RBCs and oxalate crystals. An abdominal CT scan with contrast shows linear striations radiating into the renal papillae, along with small cystic collections of contrast material in dilated collecting ducts. She is advised to increase her daily intake of fluids, and her condition improves. Which of the following renal cystic diseases is most likely to be associated with these findings?

A. Autosomal dominant polycystic kidney disease
B. Autosomal recessive polycystic kidney disease
C. Medullary sponge kidney (Correct Answer)
D. Multi-cystic renal dysplasia

Explanation: The clinical presentation and imaging findings are classic for **Medullary Sponge Kidney (MSK)**. MSK is a congenital (usually sporadic) disorder characterized by ectasia (dilation) of the pre-calyceal collecting ducts in the renal papillae [1]. **Why Medullary Sponge Kidney is correct:** * **Imaging:** The "linear striations" and "cystic collections of contrast" in the papillae are pathognomonic. On IVP or contrast CT, this is often described as a **"bouquet of flowers"** or **"paint brush"** appearance [1]. * **Clinical Features:** Patients are often asymptomatic until adulthood, presenting with **recurrent UTIs** and **nephrolithiasis** (calcium oxalate stones) [1], [3]. * **Pathophysiology:** Urinary stasis in the dilated ducts leads to stone formation. Hypercalciuria and distal renal tubular acidosis (dRTA) are common metabolic associations [3]. **Why other options are incorrect:** * **ADPKD:** Presents with large, bilateral cortical and medullary cysts that significantly increase kidney size and often lead to renal failure [2]. It does not show the specific papillary "striation" pattern. * **ARPKD:** Typically presents in infancy/childhood with bilateral enlarged kidneys and hepatic fibrosis. * **Multicystic Renal Dysplasia:** Usually a unilateral, non-genetic condition found in neonates where the kidney is replaced by large cysts and lacks a functioning pelvicalyceal system. **High-Yield Pearls for NEET-PG:** * **Diagnosis:** Best initial/traditional test is Intravenous Pyelography (IVP); CT urography is the modern standard [1]. * **Metabolic Association:** Associated with **Type 1 (Distal) RTA** and hypercalciuria [3]. * **Prognosis:** Generally benign with a normal life expectancy; management focuses on hydration to prevent stones [1]. * **Key Buzzword:** "Paint brush appearance" of the renal papillae [1].

Question 427: Central nervous system manifestations in chronic renal failure are a result of all of the following except:

A. Hyperosmolarity
B. Hypocalcemia (Correct Answer)
C. Acidosis
D. Hyponatremia

Explanation: ### Explanation In Chronic Renal Failure (CRF), central nervous system (CNS) manifestations—collectively termed **Uremic Encephalopathy**—are primarily caused by the accumulation of organic toxins, electrolyte imbalances, and metabolic disturbances. **Why Hypocalcemia is the Correct Answer:** While hypocalcemia is a hallmark of CRF (due to phosphate retention and decreased Vitamin D activation), it primarily manifests as **peripheral neuromuscular irritability** (tetany, Chvostek’s sign, Trousseau’s sign, or seizures) rather than the classic CNS depression or encephalopathy seen in uremia. In the context of this question, hypocalcemia is considered a peripheral/neuromuscular manifestation rather than a direct cause of the altered mental status characteristic of uremic CNS dysfunction. **Analysis of Incorrect Options:** * **Hyperosmolarity:** The accumulation of urea (a potent osmole) and other nitrogenous wastes increases serum osmolality. Rapid shifts in osmolarity can lead to cerebral edema or dehydration of brain cells, contributing to confusion and coma. * **Acidosis:** Metabolic acidosis (due to decreased hydrogen ion excretion) alters brain enzyme activity and intracellular pH, leading to lethargy and respiratory compensation (Kussmaul breathing) which affects CNS status [1]. * **Hyponatremia:** Impaired water excretion in CRF often leads to dilutional hyponatremia. This causes an osmotic shift of water into brain cells, resulting in cerebral edema, headache, seizures, and impaired consciousness [1]. **NEET-PG High-Yield Pearls:** * **Uremic Encephalopathy:** The earliest sign is often a loss of concentration, followed by **asterixis** (flapping tremors) and multifocal myoclonus [1]. * **Dialysis Equilibrium Syndrome:** A CNS complication occurring during or after hemodialysis caused by the rapid removal of urea, leading to cerebral edema (Reverse Urea Effect). * **Most common cause of death in CRF:** Cardiovascular disease (not renal failure itself). * **Electrolyte Rule:** CRF typically presents with **Hyper**kalemia, **Hyper**magnesemia, **Hyper**phosphatemia, and **Hypo**calcemia [2].

Question 428: In uremia, all of the following are reversed by dialysis except:

A. Sexual dysfunction (Correct Answer)
B. Pericarditis
C. Uremic lung
D. Neuropathy

Explanation: In patients with End-Stage Renal Disease (ESRD), dialysis is highly effective at removing small water-soluble toxins (like urea and creatinine) and correcting fluid overload, but it does not fully restore the complex endocrine and autonomic functions of the kidney. **1. Why Sexual Dysfunction is the Correct Answer:** Sexual dysfunction in uremia is multifactorial, involving **autonomic neuropathy, peripheral vascular disease, and endocrine disturbances** (such as hyperprolactinemia and low testosterone). Unlike fluid-based complications, these structural and hormonal changes are **not significantly reversed by dialysis**. In fact, sexual dysfunction often persists or even worsens after starting dialysis. Only successful **renal transplantation** has been shown to consistently restore hormonal balance and improve sexual function. **2. Why the other options are incorrect:** * **Pericarditis:** Uremic pericarditis is a classic **absolute indication** for starting dialysis. It is caused by the accumulation of metabolic toxins that irritate the pericardium; removing these toxins via dialysis typically resolves the inflammation. * **Uremic Lung:** This refers to pulmonary edema caused by fluid overload and increased alveolar capillary permeability. Dialysis (via ultrafiltration) removes excess fluid, rapidly resolving the "bat-wing" appearance on X-ray [1]. * **Neuropathy:** While established axonal degeneration is slow to recover, **early uremic neuropathy** (especially sensory symptoms) improves significantly with regular dialysis [2]. **Clinical Pearls for NEET-PG:** * **Indications for Dialysis (AEIOU):** **A**cidosis, **E**lectrolyte imbalance (Hyperkalemia), **I**ngestion (Toxins), **O**verload (Fluid), **U**remia (Pericarditis, Encephalopathy, Neuropathy) [2]. * **Anemia of Chronic Kidney Disease** is also not reversed by dialysis; it requires Erythropoietin (EPO) replacement [3]. * **Platelet dysfunction** in uremia (causing increased bleeding time) is reversed by dialysis and desmopressin (DDAVP).

Question 429: What is the most common metabolic abnormality predisposing patients to renal stone formation?

A. Hyperuricemia
B. Hypercalciuria (Correct Answer)
C. Distal renal tubular acidosis
D. Increased urine volume

Explanation: **Explanation:** **1. Why Hypercalciuria is Correct:** Hypercalciuria is the most common metabolic abnormality identified in patients with nephrolithiasis, found in approximately **30–60%** of stone formers. It is defined as urinary calcium excretion >250 mg/day in men or >200 mg/day in women [1]. The most frequent subtype is **Idiopathic Hypercalciuria**, a polygenic condition characterized by increased intestinal calcium absorption (absorptive) or decreased renal tubular reabsorption (renal-leak), despite normal serum calcium levels. Increased urinary calcium concentration leads to supersaturation of calcium salts (calcium oxalate/phosphate), promoting crystal nucleation. **2. Analysis of Incorrect Options:** * **Hyperuricemia (A):** While hyperuricosuria (high urine uric acid) is a risk factor for both uric acid and calcium stones, systemic hyperuricemia is less common than hypercalciuria in stone formers [1]. * **Distal Renal Tubular Acidosis (C):** Type 1 RTA is a classic cause of nephrocalcinosis and calcium phosphate stones due to alkaline urine and hypocitraturia [2]. However, it is a rare clinical entity compared to the high prevalence of idiopathic hypercalciuria. * **Increased Urine Volume (D):** This is a **protective factor**, not a predisposing abnormality. Low urine volume (dehydration) is the most common *environmental* risk factor for stone formation. **3. Clinical Pearls for NEET-PG:** * **Most common stone type:** Calcium Oxalate (specifically Calcium Oxalate Monohydrate/Whewellite). * **Most common metabolic abnormality:** Hypercalciuria. * **Most common inhibitor deficiency:** Hypocitraturia (Citrate is a potent inhibitor of calcium stone formation). * **Dietary Management:** Patients with hypercalciuria should **not** restrict dietary calcium (this increases oxalate absorption); instead, they should follow a low-sodium, low-protein diet and may be treated with **Thiazide diuretics** to reduce urinary calcium excretion [1].

Question 430: Rhabdomyolysis is seen in all of the following conditions except?

A. Hyperphosphatemia (Correct Answer)
B. Prolonged seizure activity
C. Severe hypothyroidism
D. Myopathy

Explanation: Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle fibers with the release of intracellular contents (myoglobin, CPK, and electrolytes) into the circulation. **Why Hyperphosphatemia is the correct answer:** Hyperphosphatemia is a **consequence** of rhabdomyolysis, not a cause. When muscle cells lyse, they release large amounts of intracellular phosphate into the bloodstream. Other metabolic consequences include hyperkalemia, hyperuricemia, and hypocalcemia (initially). Therefore, while it is a hallmark finding in the lab results of a patient with rhabdomyolysis, it does not trigger the condition itself. **Analysis of other options (Causes of Rhabdomyolysis):** * **Prolonged seizure activity:** Excessive muscle hyperactivity leads to an imbalance between ATP demand and supply, resulting in muscle cell death. * **Severe hypothyroidism:** Myopathy is common in hypothyroidism. In severe cases (like Myxedema coma), it can progress to frank rhabdomyolysis due to impaired muscle metabolism and reduced mitochondrial activity. * **Myopathy:** Various underlying myopathies (inflammatory like polymyositis, or metabolic like McArdle disease) predispose the sarcolemma to injury, leading to rhabdomyolysis [1]. **NEET-PG High-Yield Pearls:** * **Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Gold Standard Lab:** Serum Creatine Phosphokinase (CPK) levels >5 times the upper limit of normal. * **Renal Complication:** Acute Tubular Necrosis (ATN) caused by myoglobinuria. * **Urinalysis Clue:** Dipstick positive for blood but **microscopy negative** for RBCs (indicates myoglobinuria). * **Treatment Priority:** Aggressive IV fluid resuscitation to prevent Pigment-induced Acute Kidney Injury.

Practice by Chapter

Acute Kidney Injury

Practice Questions

Chronic Kidney Disease

Practice Questions

Glomerular Diseases

Practice Questions

Tubulointerstitial Diseases

Practice Questions

Nephrotic and Nephritic Syndromes

Practice Questions

Urinary Tract Infections

Practice Questions

Renal Replacement Therapy

Practice Questions

Fluid and Electrolyte Disorders

Practice Questions

Acid-Base Disorders

Practice Questions

Kidney in Systemic Diseases

Practice Questions

Kidney Stones and Obstructive Uropathy

Practice Questions

Hypertension in Kidney Disease

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?